This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Multiple lines of research have consistently documented sensory processing deficits in patients with schizophrenia (SP). One such deficit is poor sensory gating, in which there is an increased electrophysiological response for the second of two rapidly presented stimuli in SP compared to healthy normal volunteers (HNV). This effect is typically reported in terms of a gating ratio comparing the amplitude of the response for both the first (S1) and second (S2) stimulus (S2/S1*100). Poor sensory gating has been characterized as both a deficit in selective attention and/or in the formation of memory traces, and is a useful bio-marker of the cognitive and subsequent social dysfunction that is typically observed in SP. Although animal and invasive human studies have consistently implicated the auditory cortex, prefrontal cortex and hippocampus in mediating the sensory gating response, localized activation in these structures has not always been reported during non-invasive imaging modalities. Moreover, this deficit has been primarily been documented using electrophysiological techniques such as electroencephalography (EEG) and magnetoencephalography (MEG). To date, there has not been a single functional magnetic resonance imaging (FMRI) study that has characterized hemodynamic markers of the gating deficit in schizophrenia using the traditional gating paradigm.